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Cited by 108Stress Responses and CortisolCancer, Stress, Anesthesia, and Immune ResponseAdrenal Hormones and Disorders

Tissue-specific alterations in the glucocorticoid sensitivity of immune cells following repeated social defeat in mice

Engler, Harald, Engler, Andrea, Bailey, Michael T., Sheridan, John F.·2005·Journal of Neuroimmunology
DOI 10.1016/j.jneuroim.2005.03.002
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Abstract

Endogenous glucocorticoids (GC) play an important role in the termination of the inflammatory response following infection and tissue injury. However, recent findings indicate that stress can impair the anti-inflammatory capacities of these hormones. Lipopolysaccharide (LPS)-stimulated splenocytes of mice that were repeatedly subjected to social disruption (SDR) stress were less sensitive to the immunosuppressive effects of corticosterone (CORT) as demonstrated by an increased production of pro-inflammatory cytokines and enhanced cell survival. Myeloid cells expressing the marker CD11b were shown to play a key role in this process. Here we investigated the role of the bone marrow as a potential source of the GC-insensitive cells. The study revealed that LPS-stimulated bone marrow cells, in the absence of experimental stress, were virtually GC-resistant and retained high levels of cell viability after treatment with CORT. Recurrent exposure to the acute stressor over a period of 2, 4 or 6 days led to an increase in the GC sensitivity of the bone marrow cells. This increase in GC sensitivity was associated with enhanced mRNA expression of granulocyte-macrophage colony-stimulating factor (GM-CSF), an increase in the number of myeloid progenitors, and a decrease in the proportion of mature CD11b+ cells. The changes in the cellular composition of the bone marrow were accompanied by an increase in splenic CD11b+ cell numbers. Simultaneous assessment of the GC sensitivity in bone ma…

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  • Exposure to social cues indicating an increased risk for possible physical danger induces glucocorticoid resistance.

    “Evidence that even acute stress can alter glucocorticoid sensitivity is provided by research showing that exposure to social cues indicating an increased risk for possible physical danger induces glucocorticoid resistance.”

    From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Engler, Engler, Bailey, & Sheridan, 2005

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Authors
Engler, H., Engler, A., Bailey, M. T., & Sheridan, J. F.
Affiliations
The Ohio State University (US)
Corresponding author
Engler, Harald
ORCID
Venue
Journal of Neuroimmunology
Publisher
Elsevier BV
Published
2005-06
Volume
163
Issue
1-2
Pages
110-119
ISSN
0165-5728 (ISSN-L)
DOI
10.1016/j.jneuroim.2005.03.002
OpenAlex
W2017968071
Cited by
108
References
4
Citations by year
2026: 1 · 2024: 1 · 2023: 3 · 2022: 5 · 2021: 3 · 2020: 3 · 2019: 3 · 2018: 6 · 2017: 2 · 2016: 7 · 2015: 9 · 2014: 9 · 2013: 7 · 2012: 6
FWCI
2.78
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Journal of Neuroimmunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (R01MH046801, R01-MH46801)
  • NIH Clinical Center
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords
glucocorticoid sensitivity, corticosterone, social stress, social defeat, bone marrow, spleen, myeloid cells, CD11b, GM-CSF, myeloid progenitor cells, inflammatory cytokines, immunosuppression, stress-induced immunosuppression, tissue-specific differences
MeSH terms
Aggression, Animals, Bone Marrow Cells, Glucocorticoids, Hypothalamo-Hypophyseal System, Male, Mice, Inbred C57BL, Organ Specificity, Pituitary-Adrenal System, Spleen, Stress, Physiological, Time Factors, Mice

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